实验性脑梗死后硫酸软骨素蛋白多糖的表达  

The expression of chondroitin sulfate proteoglycans after focal cerebral infarction in hypertensive rats

作　　者：陈歆然[1] 叶兰香[1] 廖松洁[1] 龚琼[1] 余剑[1] 

机构地区：[1]中山大学附属第一医院神经内科,广州510080

出　　处：《中国神经精神疾病杂志》2014年第4期209-212,共4页Chinese Journal of Nervous and Mental Diseases

基　　金：国家自然科学基金(编号:81371276);国家自然科学基金青年项目(编号:81100871);中山大学培育青年教师基金(编号:09ykpy48)

摘　　要：目的观察高血压大鼠大脑皮质局灶梗死后病灶周围皮质及其同侧丘脑抑制性蛋白—硫酸软骨素蛋白多糖(chondroitin sulfate proteoglycans,CSPGs)的表达并探讨其对神经可塑性的可能作用。方法建立高血压大鼠的右侧大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)模型,假手术(Sham)组仅暴露而不凝闭MCA,每组24只。MCAO或Sham后第7天和第14天,各组各时间点取12只大鼠按改良神经功能缺损评分(modified neurological severity scores,mNSS)进行神经功能评分后,处死取脑,免疫荧光及western bolt检测梗死灶周围皮质及其同侧丘脑CSPGs及其组分NG2、Neurocan的表达。结果 MCAO后大鼠出现不同程度的神经功能缺损;MCAO术后第7天梗死灶周围皮质及其同侧丘脑CSPGs、NG2及全长Neurocan与Sham组相比表达均增加,并持续至第14天(P<0.05),但第7天与第14天的表达相比无统计学差异(P>0.05);术后第7天和第14天C端片段的Neurocan在上述部位的表达无统计学差异(P>0.05)。结论 CSPGs可能通过提供抑制性环境参与脑梗死后病灶局部及远隔丘脑的神经可塑性。Objective To examine the expression of inhibitory chondroitin sulfate proteoglycans （CSPGs） and in-vestigate their potential effects on neural plasticity in the peri-infarct cortex and ipsilateral thalamus after focal cerebralinfarction in hypertensive rats. Methods Twenty-four adult renovascular hypertensive Sprague-Dawley rats per groupwere subjected to permanent right middle cerebral artery occlusion（MCAO） or sham operation. Twelve rats which were se-lected randomly from per group at each time point were decapitated and their brains were removed and cut into coronalsections at 7 and 14 days post MCAO. The expression of CSPGs, NG2 and Neurocan was examined using immunostainingand western blot. Results All rats displayed neurological deficits to varying degrees and the expression of CSPGs, NG2and full length Neurocan was increased in the peri-infarct cortex and ipsilateral thalamus at 7 and 14 days （P〈0.05）.However, there were no significant difference in either expression of CSPGs, NG2 and full-length Neurocan between 7and 14 days or the expression of C-terminal fragment Neurocan at 7 and 14 days （all P〉0.05）. Conclusions CSPGs mayplay a negative role in neural plasticity through induction of inhibitory environment in the peri-infarct cortex and ipsilat-eral thalamus following focal cerebral infarction in hypertensive rats.

关 键 词：硫酸软骨素蛋白多糖 脑梗死 丘脑 神经可塑性 

分 类 号：R743.3[医药卫生—神经病学与精神病学]